Polymorphonuclear neutrophils (PMN) and monocytes from patients with acute bacterial infections (inf. PMN/MON) and cells from normal healthy controls were examined in paired studies for phagocytosis of IgG coated sheep erythrocyte targets (EIgG and EAC3bIgG). Several cellular functions of PMN were followed in longitudinal studies of inf patients, including: binding of 125I- monoclonal antibodies to Fc and C3 receptors, superoxide and myeloperoxidase production, as well as phagocytosis. PMN of infected patients expressed hyperphagocytic activity when compared with normal PMN. Phagocytic activity was prominent in inf PMN in the presence and absence of sodium azide, which regulates oxidative byproducts. Unlike inf PMN, phagocytosis was minimal in control PMN and required azide for significant expression. Superoxide, but not myeloperoxidase, was reduced in inf PMN on several days of the study, suggesting that oxidative products may play a role in the enhanced phagocytic expression in inf PMN. The number of FcR and CR3 (receptors for IgG and iC3b respectively) were similar in controls and patients, whereas CR1 (C3b receptor) was elevated on PMN of several patients. Interestingly, phagocytosis by monocytes of infected patients was similar to that of normal monocytes, unlike PMN phagocytosis which greatly exceeded that of normal PMN controls. Thus, the "down regulation" of phagocytosis seen in normal PMN is reversed in cells of patients with infections and does not occur in monocytes.